Ovarian cancer is one of the most lethal cancers. Patients usually respond very well to chemotherapy but most will eventually relapse. Many molecular processes have already been shown to influence chemotherapy resistance, including more efficient DNA repair by nucleotide excision repair. One commonly used drug for the treatment of ovarian cancer is cisplatin, a drug inducing lesions on DNA that can be repaired by NER. A previous study in our lab has shown that NER can be deficient specifically in S-phase. This effect is dependent on the kinase ATR. Thus, we chose to explore the possibility that this deficiency has an impact on resistance to cisplatin. Our objectives are: (i) to study the repair profile by NER in S-phase in ovarian cancer cell lines; (ii) to test if chemotherapeutic treatment can modulate nucleotide excision repair in cell lines by selecting cells that repair damage by NER more efficiently; (iii) to measure the sensitivity of these cell lines to cisplatin; (iv) to test if this deficiency can be attributed to ATR signalling. We show in this study that many ovarian cancer cell lines have an important defect in GG-NER specifically in S-phase. Pairs of cell lines that were isolated before and after chemotherapeutic treatment show an increase in their GG-NER efficiency in S-phase, suggesting a role for this enzymatic process in chemotherapy resistance. Also, we have found a correlation between the efficiency of GG-NER in S-phase and the sensitivity to cisplatin in the cell lines used in our study. However, the defect in GG-NER in S-phase in these ovarian cancer cell lines doesn’t seem to be due to ATR because the phosphorylation of H2AX in response to UV is equivalent between the different cell lines. This study will have an impact on our understanding of the fundamental aspects of DNA repair but could also provide insights on a potential novel mechanism of resistance to chemotherapy.